Expression data from T-cell prolymphocytic leukemia (TPLL) and normal T cells
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ABSTRACT:
ORGANISM(S): Homo sapiens
PROVIDER: GSE5788 | GEO | 2007/08/27
SECONDARY ACCESSION(S): PRJNA97145
REPOSITORIES: GEO
Similar Datasets
Project description:T-cell prolymphocytic leukemina (T-PLL) is an agressive lymphoma derived from mature T-cells, which is in most cases characterized by the presence of an inv(14)(q11q32) and a characteristic pattern of secondary chromosomal abberations. We used microarrays to compare the transcriptomes of eight immunomagnetically purified CD3+ normal donor derived peripheral blood cells with five highly purified inv(14)-positive T-PLL blood samples. Experiment Overall Design: Purified T-PLL cells and normal T-cells were analyzed on microarrays to identify differentially expressed genes. High-resolution copy number determination using SNP-chip technology and FISH in twelve inv(14)-positive T-PLL showed that differentially expressed genes clustered significantly in regions affectd by recurrent chromosomal imbalances.
2008-12-10 | E-GEOD-5788 | biostudies-arrayexpress
Project description:T-cell prolymphocytic leukemia (T-PLL) is a rare aggressive lymphoma derived from mature T cells, which is, in most cases, characterized by the presence of an inv(14)(q11q32)/t(14;14)(q11;q32) and a characteristic pattern of secondary chromosomal aberrations. DNA microarray technology was employed to compare the transcriptomes of eight immunomagnetically purified CD3+ normal donor-derived peripheral blood cell samples, with five highly purified inv(14)/t(14;14)-positive T-PLL blood samples. Between the two experimental groups, 734 genes were identified as differentially expressed, including functionally important genes involved in lymphomagenesis, cell cycle regulation, apoptosis and DNA repair. Notably, the differentially expressed genes were found to be significantly enriched in genomic regions affected by recurrent chromosomal imbalances. Upregulated genes clustered on chromosome arms 6p and 8q, and downregulated genes on 6q, 8p, 10p, 11q and 18p. High-resolution copy-number determination using single nucleotide polymorphism chip technology in 11 inv(14)/t(14;14)-positive T-PLL and 1 without the inv(14) including those analyzed for gene expression, refined chromosomal breakpoints as well as regions of imbalances. In conclusion, combined transcriptional and molecular cytogenetic profiling identified novel specific chromosomal loci and genes that are likely to be involved in disease progression and suggests a gene dosage effect as a pathogenic mechanism in T-PLL. Each Sample has its raw data file linked as a supplementary file. Experiment Overall Design: 12 T-cell prolymphocytic leukaemia samples were hybridized to 50K_Xba SNP arrays.
2008-04-10 | E-GEOD-10387 | biostudies-arrayexpress
Project description:T-cell prolymphocytic leukemia (T-PLL) is a rare aggressive lymphoma derived from mature T cells, which is, in most cases, characterized by the presence of an inv(14)(q11q32)/t(14;14)(q11;q32) and a characteristic pattern of secondary chromosomal aberrations. DNA microarray technology was employed to compare the transcriptomes of eight immunomagnetically purified CD3+ normal donor-derived peripheral blood cell samples, with five highly purified inv(14)/t(14;14)-positive T-PLL blood samples. Between the two experimental groups, 734 genes were identified as differentially expressed, including functionally important genes involved in lymphomagenesis, cell cycle regulation, apoptosis and DNA repair. Notably, the differentially expressed genes were found to be significantly enriched in genomic regions affected by recurrent chromosomal imbalances. Upregulated genes clustered on chromosome arms 6p and 8q, and downregulated genes on 6q, 8p, 10p, 11q and 18p. High-resolution copy-number determination using single nucleotide polymorphism chip technology in 11 inv(14)/t(14;14)-positive T-PLL and 1 without the inv(14) including those analyzed for gene expression, refined chromosomal breakpoints as well as regions of imbalances. In conclusion, combined transcriptional and molecular cytogenetic profiling identified novel specific chromosomal loci and genes that are likely to be involved in disease progression and suggests a gene dosage effect as a pathogenic mechanism in T-PLL. Each Sample has its raw data file linked as a supplementary file. Keywords: disease state analysis
2008-02-07 | GSE10387 | GEO
Project description:T-cell prolymphocytic leukemia (T-PLL) is a rare and aggressive neoplasm of mature T-cells with an urgent need for rationally designed therapies to address its notoriously chemo-refractory behavior. To characterize the gene expression profiles, 12 T-PLL MNC samples (>90% tumor cell content) were screened with Illumina gene expression arrays (Human HT‐12 v4 rev.2 Expression Beadchips).
2017-09-08 | E-MTAB-5916 | biostudies-arrayexpress
Project description:T-cell prolymphocytic leukemia (T-PLL) is a rare disease with rapid clinical course. Whole-exome and whole-genome sequencing have identified structural alterations in T-PLL, including inversion, translocation and copy number variation. Epigenetic alterations are the hallmark of many cancers. However, genome-wide epigenomic profiles have not been reported in T-PLL. In this study, we generated genome-wide maps of regulatory regions in both T-PLL patients and healthy individuals using H3K4me3 and H3K27ac ChIP-seq. We revealed a global alteration of both promoter and enhancer landscape in T-PLL, which supported the role of epigenetic regulation in transcriptional dysregulation of oncogenes and genes involved in DNA damage response and T-cell activation.
2021-04-20 | GSE143374 | GEO
Project description:We evaluated 13 B-PLL patient, 7 of whom were t(11;14)-positive (B-PLL+), and compared them with MCL and CLL patients.
2014-05-29 | E-MTAB-1991 | biostudies-arrayexpress
Project description:T cell prolymphocytic leukemia (T-PLL) is mostly characterized by aberrant expansion of small to medium sized pro-lymphocytes with a mature post-thymic phenotype, high aggressiveness of the disease and poor prognosis. However, T-PLL is more heterogeneous with a wide-range of clinical, morphological, and molecular features, which occasionally impedes the diagnosis. We hypothesized that T-PLL consists of phenotypic and genotypic subgroups that may explain the heterogeneity of the disease. We found that T-PLL does not show a clear skewing in T cell receptor alpha (TRA), TRB gene usage and CDR3 stereotypy. In addition, multi-dimensional immuno-phenotyping and gene expression profiling did not reveal clear T-PLL subgroups. However, based on miRNA expression profiles, T-PLL samples did clearly cluster in subgroups. We identified 35 miRNAs that were aberrantly expressed in T-PLL with miR-200c/141 as the most differentially expressed cluster. High miR-200c/141 expression was significantly correlated with increased white blood cell counts and poor survival. Furthermore, we found that overexpression of miR-200c/141 in T-PLL correlated with downregulation of their targets ZEB2 and TGFβR3, indicating that the TGFβ pathway is affected. Our results thus highlight the emerging role for aberrantly expressed oncogenic miRNAs in T-PLL, thereby paving the way for new therapeutic targets in this disease.
2021-04-02 | GSE147931 | GEO
Project description:T cell prolymphocytic leukemia (T-PLL) is mostly characterized by aberrant expansion of small to medium sized pro-lymphocytes with a mature post-thymic phenotype, high aggressiveness of the disease and poor prognosis. However, T-PLL is more heterogeneous with a wide-range of clinical, morphological, and molecular features, which occasionally impedes the diagnosis. We hypothesized that T-PLL consists of phenotypic and genotypic subgroups that may explain the heterogeneity of the disease. We found that T-PLL does not show a clear skewing in T cell receptor alpha (TRA), TRB gene usage and CDR3 stereotypy. In addition, multi-dimensional immuno-phenotyping and gene expression profiling did not reveal clear T-PLL subgroups. However, based on miRNA expression profiles, T-PLL samples did clearly cluster in subgroups. We identified 35 miRNAs that were aberrantly expressed in T-PLL with miR-200c/141 as the most differentially expressed cluster. High miR-200c/141 expression was significantly correlated with increased white blood cell counts and poor survival. Furthermore, we found that overexpression of miR-200c/141 in T-PLL correlated with downregulation of their targets ZEB2 and TGFβR3, indicating that the TGFβ pathway is affected. Our results thus highlight the emerging role for aberrantly expressed oncogenic miRNAs in T-PLL, thereby paving the way for new therapeutic targets in this disease.
2021-04-02 | GSE147932 | GEO
Project description:Epigenetic therapy overcame alemtuzumab resistance in patients with relapsed T-cell prolymphocytic leukemia and induced the expression of treatment related genes. Method: patient PBMCs from Ficoll, normal patient PBMCS enriched for CD3+/CD8+ or CD3+/CD8+/CD45RA+/CCR7- were extracted in Trizol. Conclusion: Gene expression profiles were changed by epigenetic therapy, likely activating treatment response genes silenced by carcinogenesis. Total RNA from patient Peripheral Blood Mononuclear Cells (PBMC) or from normal negatively enriched CD3+/CD8+/CCR7-/CD45RA+(CD45RO-) blood
2015-07-08 | E-GEOD-67368 | biostudies-arrayexpress
Project description:T cell prolymphocytic leukemia (T-PLL) is mostly characterized by aberrant expansion of small to medium sized pro-lymphocytes with a mature post-thymic phenotype, high aggressiveness of the disease and poor prognosis. However, T-PLL is more heterogeneous with a wide-range of clinical, morphological, and molecular features, which occasionally impedes the diagnosis. We hypothesized that T-PLL consists of phenotypic and genotypic subgroups that may explain the heterogeneity of the disease. We found that T-PLL does not show a clear skewing in T cell receptor alpha (TRA), TRB gene usage and CDR3 stereotypy. In addition, multi-dimensional immuno-phenotyping and gene expression profiling did not reveal clear T-PLL subgroups. However, based on miRNA expression profiles, T-PLL samples did clearly cluster in subgroups. We identified 35 miRNAs that were aberrantly expressed in T-PLL with miR-200c/141 as the most differentially expressed cluster. High miR-200c/141 expression was significantly correlated with increased white blood cell counts and poor survival. Furthermore, we found that overexpression of miR-200c/141 in T-PLL correlated with downregulation of their targets ZEB2 and TGFβR3, indicating that the TGFβ pathway is affected. Our results thus highlight the emerging role for aberrantly expressed oncogenic miRNAs in T-PLL, thereby paving the way for new therapeutic targets in this disease. We used gene expression profiling by microarray to determine gene expression differences between T-PLL samples and normal T-cell subets.
2021-04-02 | GSE147930 | GEO